Evidence map›Paper›PMID 39308860›Full record

ArticleFrontiers in immunology2024

Novel AHR ligand AGT-5 ameliorates type 1 diabetes in mice through regulatory cell activation in the early phase of the disease.

Natalija Jonić, Ivan Koprivica, Stavroula G Kyrkou, Vasileios-Panagiotis Bistas, Christos Chatzigiannis, Nataša Radulović, Ivan Pilipović, Andjelina Jovanović, Milan B Jovanović, Mirjana Dimitrijević and 2 more

Abstract read
In one paragraph

Article in Frontiers in immunology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.

0numbers the graph read from it
0cells of the map it votes in
8citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

8 citing papers in PubMed.

  1. Article
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

12 authors.

Natalija JonićDepartment of Immunology, Institute for Biological Research "Siniša Stanković" - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Ivan KoprivicaDepartment of Immunology, Institute for Biological Research "Siniša Stanković" - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Stavroula G KyrkouSection of Organic Chemistry & Biochemistry, Department of Chemistry, University of Ioannina, Ioannina, Greece.
Vasileios-Panagiotis BistasSection of Organic Chemistry & Biochemistry, Department of Chemistry, University of Ioannina, Ioannina, Greece.
Christos ChatzigiannisSection of Organic Chemistry & Biochemistry, Department of Chemistry, University of Ioannina, Ioannina, Greece.
Nataša RadulovićDepartment of Immunology, Institute for Biological Research "Siniša Stanković" - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Ivan PilipovićDepartment of Immunology, Institute for Biological Research "Siniša Stanković" - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Andjelina JovanovićDepartment of Otorhinolaryngology with Maxillofacial Surgery, Clinical Hospital Center "Zemun", Belgrade, Serbia.
Milan B JovanovićDepartment of Otorhinolaryngology with Maxillofacial Surgery, Clinical Hospital Center "Zemun", Belgrade, Serbia.
Mirjana DimitrijevićDepartment of Immunology, Institute for Biological Research "Siniša Stanković" - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.
Andreas G TzakosSection of Organic Chemistry & Biochemistry, Department of Chemistry, University of Ioannina, Ioannina, Greece.
Ivana StojanovićDepartment of Immunology, Institute for Biological Research "Siniša Stanković" - National Institute of the Republic of Serbia, University of Belgrade, Belgrade, Serbia.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Type 1 diabetes (T1D) is an autoimmune disease with a strong chronic inflammatory component. One possible strategy for the treatment of T1D is to stimulate the regulatory arm of the immune response, i.e. to promote the function of tolerogenic dendritic cells (tolDC) and regulatory T cells (Treg). Since both cell types have been shown to be responsive to the aryl hydrocarbon receptor (AHR) activation, we used a recently characterized member of a new class of fluorescent AHR ligands, AGT-5, to modulate streptozotocin-induced T1D in C57BL/6 mice. Prophylactic oral administration of AGT-5 reduced hyperglycemia and insulitis in these mice. Phenotypic and functional analysis of cells in the pancreatic infiltrates of AGT-5-treated mice (at the early phase of T1D) revealed a predominantly anti-inflammatory environment, as evidenced by the upregulation of tolDC and Treg frequency, while CD8

Indexed as

Dendritic CellsDiabetes Mellitus, Type 1Mice, Inbred C57BLReceptors, Aryl HydrocarbonT-Lymphocytes, RegulatoryAnimalsDiabetes Mellitus, ExperimentalFemaleHumansIndoleamine-Pyrrole 2,3,-DioxygenaseLigandsLymphocyte ActivationMiceIndoleamine-Pyrrole 2,3,-DioxygenaseLigandsReceptors, Aryl Hydrocarbonaryl hydrocarbon receptor (AhR)gut-associated lymphoid tissue (GALT)insulitislamina propriaT regulatory cell (TREG)type 1 diabetes (T1D)

Identifiers

PMID39308860
PMCPMC11412818

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.